THE SPLEENCHAPTER OUTLINE:

o The Spleeno Embryology & Anatomyo Physiology & Pathophysiologyo Splenectomy Techniques

Px Preparation Open Splenectomy Laparoscopic Splenectomy Partial Splenectomy Inadvertent Intraoperative Splenic Injury

o Indications for Splenectomy RBC Disorders

Congenital Acquired

WBC Disorders Chronic Lymphocytic Leukemia Hairy Cell Leukemia Hodgkin's Disease Non-Hodgkin's Lymphoma

Platelet Disorders Idiopathic Thrombocytopenic Purpura Thrombotic Thrombocytopenic Purpura

Bone Marrow (Myeloproliferative) Disorders Chronic Myeloid Leukemia Acute Myeloid Leukemia Chronic Myelomonocytic Leukemia Essential Thrombocythemia Polycythemia Vera Myelofibrosis (Agnogenic Myeloid Metaplasia)

Cysts & Tumors Infections & Abscesses Storage & Infiltrative Disorders

Gaucher's Disease Niemann-Pick Disease Amyloidosis Sarcoidosis

Misc. Disorders & Lesions Splenic Artery Aneurysm Portal Hypertension Felty's Syndrome

o Imaging: Size & Pathology Ultrasound Computed Tomography Plain Radiography Magnetic Resonance Imaging Angiography Nuclear Imaging Splenic Index

o Preoperative Considerations Vaccination Splenic Artery Embolization Deep Vein Thrombosis Prophylaxis

o Splenectomy Outcomes Complications Hematologic Outcomes Overwhelming Postsplenectomy Infection

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INTRODUCTIONEmbryology & AnatomySPLEENA. Embryology of the Spleen

o Arises from the MESODERM between 1-2 Months Gestationo Becomes evident on the 5th Week of Gestation in an 8mm Embryo

- encapsulated mass + lymphoid tissue- largest reticuloendothelial organ in the body- origin: primitive mesoderm (as an outgrowth of the L side of the dorsal mesogastrium)- 5th wk of gestation: 8mm long

B. Anatomy of the Spleeno It is a Multifauceted Organ o It is in Close Association with the Pancreas, Left Kidney, Stomach, Transverse Colono Superior to the Spleen is the DIAPHRAGMo Located in the 9th ICS (L1) – at the level of the Left Mid-Axillary Lineo (+) Anterior Notch

1. Dimensions of the Spleen 10 cm Long (7-11cm long) Weight = 100g (in Filipinos) TO be Palpable (Splenomegaly) = Size has to be DOUBLED!

2. Accessory Spleen Most Common ANOMALY of Splenic Embryology 80% are found in the Region of the Splenic Hilum and Vascular Pedicle

3. Splenomegaly (prenotes) Spleen weighing 500mg or more and/or 15cm (or more) in Length

- final location: LUQ; smooth, diaphragmatic surface facing posterosuperiorly- abdominal surface of the diaphragm separates the spleen from the lower left lung and pleura and the 9th-11th ribs- visceral surface faces the abdominal cavity and contains gastric, colic, renal, and pancreatic impressions- superior border of the spleen: separates the diaphragmatic surface from the gastric impression of the visceral

surface and often contains 1 or 2 notches (particularly pronounced when the spleen is greatly enlarged)- ave. audult spleen: 7-11cm in length & weights 150g (70-250g)- Splenomegaly:

Moderate, massive, hyper≥500g and/or averaging ≥15cm in lenghmassive: >1kg in mass or >22cm in lengthat least 2x the normal size: spleens palpable below left costal margin; est. ≥750gmay result in sequestration of up to 80% of the platelet pool

- most common anomaly: accessory spleen (20% of population; 30% of Px w/ hematological disease)- locations of accessory spleen in descending order of frequency:

1. region of the splenic hilum & vascular pedicle (80%)2. gastrocolic ligament3. pancreas tail4. greater omentum5. stomach’s greater curve6. splenocolic ligament7. small & large bowel mesentery8. left broad ligament in women9. left spermatic cord in men

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C. Four Cardinal Ligaments (Suspensory Ligaments that Support the Spleen)o Stomach = GASTROSPLENIC (it is the ONLY Vascular Ligament of the Spleen)o Colon = Splenocolic Ligament o Diaphragm = Phrenosplenic Ligamento Kidney, Pancreas = Splenorenal Ligament

**NOTE: Gastrosplenic is the ONLY Vascular Ligament It contains Short Gastric Vessels The others are NOT Vascular

- of particular clinical relevance: the spleen is suspended in position by several ligaments and peritoneal folds:1. to the colon: Splenocolic ligament2. to the stomach: Gastrosplenic ligament – contains the short gastric vessels, the remaining ligaments are

avascular, with rare exceptions, such as in patients with portal hypertension3. to the diaphragm: Phrenosplenic ligament4. to the kidney, adrenal gland, tail of the pancreas: Splenorenal ligament

**cadaveric normal series: the tail of the pancreas has been demonstrated to lie w/n 1cm of the splenic hilum 75% of the time and in 30% of patients actually to abut the spleen

D. Vasculature of the Spleen o Splenic Artery = Comes from the CELIAC AXIS - where the spleen derives most of its bloodo Short Gastric Vessels = from the LEFT GASTROEPIPLOIC ARTERY running w/n the gastrosplenic

ligamento Splenic Vein = joins the Superior Mesenteric Vein to form the Portal Vein and accommodates the major

venous drainage of the spleen

1. Splenic Artery Provides Majority of the Blood Supply It is the FIRST Branch of the Celiac Artery LARGEST and Most TORTUOUS Branch of the three main branches of the Celiac Artery Types according to the pattern of its terminal branches

a) distributed type – most common – 70% - distinguished by a short trunk with many long branches entering over ¾ of the spleen’s medial surface

b) magistral type – 30% - has a long main trunk dividing near the hilum into short terminal branches, and these enter over 25%-30% of the spleen’s medial surface

Blood Flow through the Spleen:

Celiac Artery

Splenic Artery

SPLEEN

Splenic Vein

Combines with the Superior Mesenteric Vein

Portal Vein

2. Short Gastric Vessels Provides a SMALL amount of Blood to the Spleen

3. Splenic Vein Accommodates the Major Venous Drainage of the Spleen Runs retropancreatically as it fuses with the Superior Mesenteric Vein to form the Portal Vein

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In Patients with Portal Hypertension = there is ENLARGEMENT of the Splenic Vein and even the SPLEEN itself (Splenomegaly)

E. Histology of the Splenic Parenchyma***when a normal, freshly excised spleen is sectioned, the cut surface is finely granular and predominantly dark red with whitish nodules distributed liberally across its expanse – reflects microstructure

1. Outer Red Pulp Contains the Venous Sinuses (drain into tributaries of the Splenic Vein) – surrounded and

separated by the reticulum (a fibrocellular network of collagen fibers and fibroblasts; appear as splenic cords) – lined by long, narrow endotheial cells that are variably in close apposition to one another or are separated by intercellular gaps in a configuration unique to the spleen

Macrophages – w/n the reticulum – remove microorganisms, cellular debris, antigen-antibody complexes, and senescent erythrocytes from the circulation

Comprises ~75% of the Total Splenic Volume Serves as a DYNAMIC FILTRATION System

2. Marginal Zone (Interface) At the junction of the Red and White Pulp; Intertwines the Red and White Pulp Lymphocytes - loosely aggregated in this zone Blood is derived from this zone to the Red Pulp, where lymphocytes & locally produced

immunoglobulins ultimately enter the systemic circulation Narrow; Contains the Plasma Cells and Macrophages Also with FILTERING Function

3. Inner White Pulp Has Immunologic Function (for IMMUNOLOGIC Function) Consists of Collagen and Malphigian Follicles Consists of nodules that are normally ≤ 1mm in size but can increase to several cm when nodules

coalesce (as occurs in certain lymphoproliferative disorders)

**Periarticular Lymphatic Sheath - around the terminal mm of splenic arterioles; replaces the native adventitia of the vessel; composed of T lymphocytes & intermittent aggregations of B lymphocytes or lymphoid follicles **Follicles – when stimulated: centers of lymphocyte proliferation develop germinal centers regress as the stimulus/infection subsides**blood flow: arteriesarterioleswhite pulpmarginal zonered pulp

II. PHYSIOLOGY OF THE SPLEEN: **”Defense Spleen” Filtration Host Defense Storage Cytopoiesis

A. Filtration (Capsule of the Spleen: 1-2mm thick; rich in Collagen & Elastin fibers)o Most IMPORTANT Function, along with providing Immunity, of the Spleeno It filters the Dead Red Blood Cells (it clears damaged or aged blood cells, removes abnormal WBCs and

Platelets and some Foreign Bodies)o Mostly via the slower/open circulation – blood percolates through the reticular space and splenic cords,

thus gaining access through gaps/slits in the endothelial cell lining to the sinuses **blood is exposed to extensive contact with splenic macrophages

o Selective slowing of blood cell flow vs. plasma flow: within the spleen the erythrocte conc. (hematocrit) is 2x that of the general circulation

o Recall: Lifespan of RBC = 120 days (2 days spent sequestered in the spleen)o It is the “Graveyard of the RBCs” = approximately 20mL of Aged RBCs are removed DAILY

B. Immunologic Function (Host Defense)o Contribute to BOTH Humoral and Cell-Mediated Immunity

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o Antigens – filtered in the white pulp; presented to immunocompetent centers w/n the lymphoid follicles; elaboration of immunoglobulins (predominantly Immunoglobulin M)

o Antigen challengeacute immunoglobulin M responserelease of Opsonic antibodies from the white pulpantigen clearance (facilitated by the splenic & hepatic reticuloendothelial systems

o Opsonins, Tuftsins, Properidin are manufactured in the Spleen o Properidin = Initiator of the Alternate Pathway of Complement Activationo Site of blood borne antigen presentation and the initiation of T and B lymphocyte activities

involved in humoral and cellular immune responses

C. Storageo Storage for Cellular Elements such as RBC, WBS, etc

D. Hematopoiesiso In the Fetal Stage, the Spleen is responsible or Hematopoiesiso The Spleen plays a MINOR Role in the Human Fetus beginning in the 4th month o Splenic Hematopoiesis = abnormal RBCs in adults w/ myeloproliferative disorders

**Chronic hemolytic disorders – tissue may become permanently hypertrophiedreticular spaces of the red pulp become distended w/ macrophages engorged w/ the products of erythrocyte breakdownsplenomegaly**splenomegaly: abnormal enlargement of the spleen; hypersplenism: presence of one or more cytopenias in the context of a normally functioning bone marrow**disorders causing hypersplenism:

1. those w/ destruction of abnormal blood cells (occurs in an intrinsically normal spleen)2. primary disorders of the spleen = sequestration and destruction of normal blood cells

**hypersplenism = neutropenia through sequestration of normal wbc or the removal of abnormal ones**platelets: survive in circulation for 10days; normally 1/3 of the platelet pool is sequestered in the spleen**excessive sequestration of platelets or platelet destruction in the spleen = thrombocytopenia

III. DIAGNOSTIC TEST FOR SPLENIC EVALUATION**indications: trauma, LUQ pain, splenic lesions (tumors, cysts, abscesses), guidance for percutaneous procedures

A. Ultranosographyo 2D Ultrasound will suffice to identify Shape, Size, Adjacent Structureso Advantage = COST EFFECTIVE and Readily Available!o It is NOT Invasive and does NOT expose the Patient to Ionizing Radiationo One of the Most Commonly Usedo Often the 1st imaging modality used for eveluation/resuscitation of a trauma pxo Percutaneous UTZ guided procedures for splenic disease (ei cyst aspiration, bipsy)o detection of textural lesions

B. CT-Scano Main Advantage = HIGHER Resolution it gives (gives a more detailed appearance of the Splenic

Parenchyma)o Automated, less operator dependento Evaluation & management of the blunt trauma Pxo It delineates the Adjacent Structures BETTER, compared to an Ultrasoundo It uses Iodinated Contrast Material to add Diagnostic Clarity (small but real risks of renal impairment,

allergic rxns)

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NOTES from Prenotes: 5th to 8th Month = Spleen contributes Actively to the Production of BOTH RBCs and WBCs that enter

the Circulation (does NOT Continue into Adulthood) Spleen is the LARGEST Reticuloendothelial Organ in the Body Total Splenic Inflow of Blood = 250-300mL/min Humans have Fast/closed circulation: arteriolesvenous sinuses; slower/open circulation

**Nontrauma: CT-Scan is useful in: Assessment of Splenomegaly Identification of Splenic Lesions Guidance for Percutaneous Procedures

C. MRIo Excellent detail and versatility in abdominal imagingo Cost is also HIGH!o It is reserved for difficult cases when CT-Scan CANNOT determine the Pathology

D. Radioscintigraphy (Nuclear Imaging)o Identification of ACCESSORY SPLEENo Uses Technetium-99 and Sulfur Colloids which are given IV (then it becomes concentrated in the

Accessory Spleen)

E. Plain Radiography (X-Ray)o Visualization of ORGAN DISPLACEMENT adjacent to the Spleeno RARELY used alone for Splenic Imaging o Can provide an Outline of the Spleen in the LUQ or Suggest Splenomegaly by revealing Displacement of

the Adjacent air-filled Structureso May Demonstrate Splenic CALCIFICATIONS: a non specific finding; phlebolith, splenic artery

aneurysm, sickle cell changes, tumors, echinococcosis, TB

F. Angiographyo Outlining the Vascular Supplyo Invasive arterial imaging; localization and Tx of hemorrhage in select trauma Px, delivery of a variety of

therapies in Px with cirrhosis or portal and sinistral hypertension, and in transplant Px, adjunct to splenectomy for tx of hematologic disorders such as ITP or hypersplenism, preoperative or intraoperative SAE for elective splenectomy

G. Splenic Indexo Obtained by multiplying the spleen’s length, width, and height and using these values in a specific

standard ellipsoid volume and linear regression formulao Normal values: 120mL-480mL o Normal ex vivo wt. = 150g

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IV. GENERAL INDICATIONS FOR SPLENECTOMY (check Table 34-1: page 1250) Most Common Indication for Splenectomy = TRAUMA to the Spleen Most Common Indication for ELECTIVE Splenectomy = (in the past) staging for Hodgkin’s Disease, (more

recently) ITP

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>>RED BLOOD DISORDERSCONGENITAL

RBC Enzyme DeficienciesHereditary Sperocytosis Pyruvate Kinase Deficiency Glucose-6-Phosphate Dehydrogenase

DeficiencyIndications for Splenectomy

- hemolytic anemia- recurrent transfusions- intractable leg ulcers

Indications for Splenectomy- only in severe cases- recurrent transfusions

Indications for Splenectomy- None

Response- improves/eliminates anemia

Response- transfusion

requirement- palliative only- in severe cases,

splenectomy can alleviate transfusion requirements

Response-

Autosomal dominant Involved in glycolytic pathways Needed to maintain a high ratio of reduced to oxidized glutathione in the RBC, protecting it from oxidative damage

Most common hemolytic anemia for w/c splenectomy is indicated

Most common RBC deficiency to cause congenital chronic hemolytic anemia

Most common RBC enzyme deficiency overall

Results from an inherited dysfunction or deficiency in one of the erythrocyte membrane proteins

- spectin- ankyrin- band 3 protein- protein 4.2

destabilization of the lipid bulayer = pathologic release of membrane lipids

Pathophysiology is unclear

RBC: more spherical, less deformable shapeSpherocytic erythrocytes are sequestered and destroyed in the spleen

- mild jaundice- splenomegaly- varying degrees of anemia

(severe: 4-6 g/dL)

- transfusion dependent severe anemia in early childhood

- well compensated mild anemia in adolescents or adults

- splenomegaly is common

- chronic hemolytic anemia- acute intermittent hemolytic episodes- no hemoysis ( depend on the variant of

G6PD def.)

- mean corpuscular volume: low to normal or slightly decreased

- screening: mean corpuscular hemoglobin concentration + erythrocyte distribution width

- reticulocyte count- lactate dehyrogenase level- level of UNconjugated bilirubin- (+) spherocytes

- specific mutations at the complementary DNA or genomic level

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- timing of splenectomy: impt; aimed at possibility of overwhelming postsplenectomy sepsis

- delay operation until the px is between 4-6yo (unless the anemia and hemolysis accelerate)

- gallstones are more likely to dev. In px w/ HS

- for children w/ cholelithiasis – prophylactic cholecystectomy is

- splenectomy should be delayed if possible to at least 4yo to risk of postsplenectomy infection

- mainstay of Tx: avoidance of drugs known to precipitate hemolysis in px w/ G6PD deficiency

- tranfusions are given in case of symptomatic anemia

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recommended at the time of splenectomy

ACQUIREDWarm-Antibody Autoimmune Hemolytic

AnemiaHemoglobinopathies: sickle cell disease Thalassemia: (alpha, beta, gamma)

Indications for Splenectomy- failure of medical (steroid) therapy-

Indications for Splenectomy- Hx of acute sequestration crisis

(painful enlargement of the spleen, circulatory collapse)

- Splenic Sx (hypersplenism, splenic abscess)

- Infarction (consider concomitant cholecystectomy)

Indications for Splenectomy- excessive transfusion requirements- symptomatic splenomegaly- infarction

Response- 60-80% response rate- recurrences common

Response- palliative- variable response

Response- transfusion requirements- relief of symptoms

Autosomal codominant (inherited from 1 parent(heterozygous): carriers; both parents (homozygous):sickle cell anemia)Inherited schronic hemolytic anemia that results from the mutant sicle cell hemoglobin (HbS) w/n the rbc

Mendelian recessive

AIHA is classified as either primary or secondary; also classified as warm (discussed in the chapter) or cold (based on the temp. at w/c the autoantibodies exert their effect)**cold: Sx are uncommon and splenectomy is almost never indicatedMore common among women, mostly idopathic Most common genetic diseases known to arise

from a single gene defectCharacterized by the destruction of RBCs, whose erythrocytic life span is diminished by autoantibodies leveled against antigens

The underlying abnormality is the mutation of adenine to thymine in the 6th codon of the Beta-hemoglobin gene substitution of valine for glutamic acid as the 6th amino acid of the beta-globin chain

In all forms thalassemia the primary defect is absent or reduced production of hemoglobin chains

- acute or gradual presentation- mild jaundice- signs ans sx of anemia- 1/3- ½ (splenomegaly)

- microvascular congestion thrombosis ischemia tissue necrosis

- early splenomegaly infarction of the spleen autosplenectomy

- hemolysis as indicated by anemia- reticulocytosis- products of rbc destruction- bilirubin in the blood, urine and stool- (+) Coomb’s test = confirms the AIHA

Dx by distinguished autoimmune from other forms of hemolytic anemia

- painful intermittent episodes

- tx depends on severity; primary vs secondary

- prompt attention, rbc transfusion for severe symptomatic anemia

- mainstay tx: corticosteroids- cont. therapy til hematocrit and

reticulocyte count (usually w/n 3wks)

- splenectomy doesn’t affect the sickling process

- therapy largely palliative- transfusions indicated for anemia,

moderately severe episodes of of acute chest syndrome (new infiltrate on CXR, new sx like fever, cough, sputum production or hypoxia) & pre-op before splenectomy

- (+) stroke, severe crisis = hydration, exchange transfusion(manually or automated apheresis equipment)

- hydroxyurea – an oral chemotherapeutic agent that upregulates fetal hemoglobin, w/c interferes w polymerization of HbS = sickling process

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>>WHITE BLOOD CELL DISORDERSChronic Lymphocytic

LeukemiaHairy Cell Leukemia Hodgkin’s Disease Non-Hodgkin’s Lymphoma

Indications for Splenectomy- cytopenias- anemia

Indications for Splenectomy- cytopenias- symptomatic

splenomegaly

Indications for Splenectomy- surgical staging in select cases

Indications for Splenectomy- cytopenias- symptomatic

splenomegalyResponse

- 75% response rateResponse- 40-70% response rate

Response-

Response- improved cbc values- relief of symptoms

Main characteristic: progressive accumulation of long-lived but nonfunctional lymphocytes

Main characteristic:(+) splenectomy, pancytopenia, large numbers of abnormal lymphocytes in the bone marrow; An uncommon blood disorder, 2% of all adult leukemias;Irregular hair like cytoplasmic projections identifiable on the peripheral smear

Main characteristic:(+) Reed-sternberg cells;

4 major histo types:- lymphocyte

predominance type- nodular sclerosis type- mixed cellularity type- lymphocyte depletion

type

Encompasses all malignancies derived from the lymphoid system except classic HD;Proliferation of any one of the 3 predominant lymph cell types – NK cells, T cells, B cells – may be included in the category of NHL

Classifications:- nodal / extranodal- indolent / aggressive /

very aggressiveSymptoms

- nonspecific- weakness- fatigue- fever w/o illness- night sweats- frequent bacterial and

viral infections- most frequent finding:

lymphadenopathy- (+) splenomegaly:

may be massive or barely palpable below the costal margin

Few symptoms;Require no specific therapy

- >90% of px – (+) lymphadenopathy above the diaphragm

- lymph nodes can become become bulky in the mediastinum = shortness of breath, cough, obstructive pneumonia,

- spleen: an occult site of spread; massive splenomegaly is not common

- clinical manifestations vary

1. indolent lymphomas – mild or no symptoms and seek medical attention for a swollen lymph node

2. aggressive/very aggressive – pain, swelling due to obstruction of vessels, fever, and night sweats

Splenectomy may facilitate chemotherapy in px whose cell counts were prohibitively low before spleen removal;Palliative splenectomy also indicated for symptomatic splenomegaly

Splenectomy doesn’t correct the underlying disorder but does return cell counts to normal in 40-70% of patients and alleviates sx of splenomegaly

Staging information affects tx because px with early stage disease who have no splenic involvement may be candidates for radiotherapy alone; (+) splenic involvement: chemotherapy or multimodality therapy

Splenectomy is indicated for management of symptoms related to an enlarged spleen as well as for improvement of cytopenias;Surgical staging not indicated

**Hodgkin’s Disease- histologic type, location, symptomatology – influence survival for px with HD

Stage I - limited to 1 anatomic regionStage II – presence of 2 or more contiguous or noncontiguous regions on the same side of the diaphragmStage III – involves disease on both sides of the diaphragm, but limited t lymph nodes, spleen and

Waldeyer’s ring (the ring of lymphoid tissue formed by the lingual, palatine, and nasopharyngeal tonsils)

Stage IV – involvement of the bone marrow, lung, liver, skin, GI tract, or any organ or tissue other than the lymph nodes or Waldeyer’s ring

- current indications for surgical staging: clinical stage I or II disease of the nodular sclerosing type and no symptoms referable to HD

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- surgical staging procedure for HD includes a bipsy of the liver, splenectomy, and the removal of representative nodes and the retroperitoneum, mesentery, and hepatoduodenal ligament; an iliac marrow biopsy is geereally included

>> PLATELET DISORDERSIdiopathic Thrombocytopenic Purpura Thrombocytic Thrombocytopenic Purpura

Indications for Splenectomy- failure of medical therapy- recurrent disease

Indications for Splenectomy- excessive plasma exchange requirement

Response- 75-85% rate of long term response

Response- typically curative

- also called immune thrombocytopenic purpura- an autoimmune disorder characterized by platelet count and

mucocutaneous and petechial bleeding. - platelet count stems from premature removal of platelets opsonized by

antiplatelet IgG autoantibodies produced in the spleen. - Adult onset and childhood onset ITP are strikingly different in their clinical

course and management.- (+) petechiae or ecchymosis, although some will experience major bleeding

from the outset. - Bleeding may occur from mucosal surfaces in the form of gingival bleeding,

epistaxis, menorrhagia, hematuria, or even melena. - >50,000/mm3 ---incidental findings- between 30,000 and 50,000/mm3 --- easy bruising- 10,000-30,000/mm3 --- spontaneous petechiae or ecchymoses- <10,000/mm3 are at risk for internal bleeding. - major intracranial hemorrhage is about 1 %, usually occurring early in the

disease course- Children: often present at a young age (peak age approx. 5 years) with

sudden onset of petechiae or purpura several days to weeks after an infectious illness

- Adults: more chronic form of disease with an insidious onset- Splenomegaly with ITP is uncommon in both adults and children, and its

occurrence should prompt a search for a separate cause of thrombocytopenia.

- 10% of children have a palpable spleen tip

- a serious disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and neurologic complications.

- Abnormal platelet clumping occurs in arterioles and capillaries, reducing the lumen of these vessels and predisposing the patient to microvascular thrombotic episodes

- lumen size = shearing stresses on erythrocytes = deformed RBCs hemolysis

- underlying abnormality is likely related to the persistence of unusually large multimers of von Willebrand factor associated w/ platelet clumping int the Px blood

- Clinical features of the disorder include petechiae, fever, neurologic symptoms, renal failure, and infrequently cardiac symptoms, such as heart failure or arrhythmias.

- Petechial hemorrhages in the lower extremities are the most common presenting sign.

- Fever + flu-like Sx (malaise, fatigue)- Neurologic changes range from generalized

headaches to altered mental status, seizures, and even coma.

- (+) petechiae and thrombocytopenia diagnosis of TTP consideration of treatment

Diagnosis- exclusion of other possibilities in the presence of platelet count and

mucocutaneous bleeding- other diseases = secondary forms of ITP: systemic lupus erythemaous,

antiphospholipid syndrome, lymphoproliferative disorders, HIV infections and hepatitis C should be identified and treated when present

- Hx of drugs known to cause thrombocytopenia- (+) megathrombocytes on peripheral smear

Diagnosis- confirmed by peripheral blood smear- (+) schistocytes, nucleated RBCs, basophilc

stippling- (-) Coomb’s test (to differentiate from Evan’s

syndrome, SLE)

Therapy- usual 1st line therapy: oral prednisone (1.0-1.5mg/kg per day)- IV immunoglobulin: (1.0g/kg per day for 2-3 days) – indicated for internal

bleeding when platelet counts remain <5,000/mm3 or (+) extensive purpura – thought to impair clearance of immunoglobulin G-coated platelets by competing for binding to tissue macrophage receptors (immediate response is common, sustained remission is not

- Splenectomy – indicated for failure od medical tx, prolonged use of steroids w undesirable effects, most cases of 1st relapse

- Persistent need for > 10-20 mg/d for 3-6months to maintain a platelet count of >30,000/mm3 splenectomy

- Children w/ typical ITP obervation + short term therapy in select cases- Urgent splenectomy if severe in both children and adults

Therapy- first line therapy: plasma exchange (daily removal of

a single volume of the px’s plasma + its replacement w/ fresh frozen plasma until the Sx are corrected; 1-2wks

- splenectomy: if (+) relapse; (+) multiple exchanges; well tolerated w/o significant morbodity

Outcomes- splenectomy – permanent response w/o subsequent need for steroids in 75-

85% of px- responses usuallu occur w/n the first post op wk- for px w extremely platelet counts (<10,000/mm3), platelets should be

available for surgery but should not be given pre-op- once the splenic pedicle is ligated platelets are given if (+) cont. bleeding

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>>BONE MARROW (MYELOPROLIFERATIVE) DISORDERS- characterized by an abnormal growth of cell lines in the bone marrow- common underlying problems leading to splenectomy: symptomatic splenomegaly- Splenomegaly Sx: early satiety, poor gastric emptying, heaviness or pain in the LUQ, and even diarrhea- Hypersplenism in these conditions: usually associated with splenomegaly- Splenectomy usually performed- Splenomegaly sometimes treated nonsurgically by chemotherapeutic agents (busulfan, hydroxyurea, interferon-alpha) mild to moderate

size reductions and some relief of Sx (discontinuation=rapid splenic regrowth)- Radiation: only used when splenectomy is not an option

Chronic Myeloid Leukemia

Indications for Splenectomy:

Symptomatic splenomegaly

Response:

Relief of abdominal pain and early satiety

- disorder of the primitive pluripotent stem cell in the bone marrow = significant erythroid, megakaryotic, and pluripotent progenitors in the peripheral blood smear

- genetic hallmark: transposition between the bcr gene on chromosome 9 and the abl gene on chromosome 22

- 7-15% of all leukemias- often asymptomatic but can cause fatigue, anorexia, sweating and LUQ pain, early satiety

due to splenomegaly- (+) splenomegaly in 50% of CML Px- Tx: splenectomy=to ease pain and early satiety

Acute Myeloid Leukemia

Intolerable symptomatic splenomegaly

- abnormal growth of stem cells in the bone marrow- unlike CML, has a more rapid and dramatic presentation- hematopoietic stem cells in the bona marrow = inhibition of growth and maturation of

normal RBCs, WBCs, and plateletsDeath w/n wks-months if left untreated- 1.2% of all cancer deaths- viral-like illness w/ fever, malaise, bone pain due to expansion of the meduallry space- Splenectomy: indicated only in the uncommon circumstance that LUQ pain and early

satiety become unbearable; weight benefits vs. risk in immunocompromised px due to neutropenia and chemotherapy

Chronic Myelomonocytic

Leukemia

Symptomatic splenomegaly

- characterized by a proliferation of hematopoietic elements in the bone marrow and blood- differs from CML in that it is associated w/ monocytosis in the peripheral smear (>1x10^3

monocytes/mm3) and in the bone marrow- (+) splenomegaly in 50% of CMML px- splenectomy= symptomatic relief

Essential Thrombocytopenia

Only for advanced disease

- abnormal growth in the megakaryocyte cell line = platelets in the blood stream- Dx made after exclusion of other chronic myeloid disorders w/ thrombocytosis- Vasomotor sx, thrombohemorrhagic events, recurrent fetal loss, tranformation to

myelofibrosis w/ myeloid metaplasia or AML- Hydroxyurea=thrombotic events in ET but doesn’t alter transformation to myelofibrosis or

leukemia- (+) splenomegaly in one third to 50% of ET Px- splenectomy not useful in early stages; reserved for later stages when myeloid metaplasia

has developed- select px carefully-significant bleeding reported to complicate splenectomy

Polycythemia Vera - clonal, chronic, progressive myeloproliferative disorder characterized by RBC mass; (+)leukocytosis, thrombocytosis, splenomegaly

- longer survival but still at risk for transformation to myelofibrosis or AML- rare; annual occurance of 5-17 cases per million pop- ruddy cyanosis, conjuctival plethora, hepatomegaly, splenomegaly, hypertension- Tx: tailored to risk status of px; phlebotomy, aspirin, chemotherapeutic agents- Splenectomy not helpful in early stages; reserved for later stages when myeloid metaplasia

has developed or if splenomegaly Sx are unbearableMyelofibrosis

(Agnostic Myeloid Metaplasia)

Severe symptomatic splenomegaly

76% clinical response at 1yr, high risk of hemorrhagic, thrombotic, infectious complications (26%)

- response to a clonal proliferation of hematopoietic stem cells- marrow failure is common- true incidence unknown- excessive radiation may play a role: proximity to Japan bombing and Thorotrast (contrast

agent thorium dioxide) = incidence- Dx: examination of peripheral blood smear + bone marrow; nucleated RBCs, immature

myeloid elements in the blood (96% of the cases); teardrop poikilocytosis; exclude Hx of primary neoplasm (lymphoma, adenocarcinoma of other organs) or TB-these px may develop secondary myelofibrosis

- Tx: asymptomatic(observation); symptomatic (therapeutic intervention); splenomegaly-related sx (splenectomy); medical Tx also an option

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- Thorough pre-op workup must precede splenectomy:1. acceptable cardiac, pulmonary, hepatic,, renal reserve for the operation2. examine coagulation system (test factor V and VIII and fibrin split products, platelet

count, bleeding time)- platelet counts = adrenal steroids and/or platelet transfusion at the time of surgery- complications post-splenectomy more common compaired to other hematologic indications- thrombosis, hemorrhage, and infection complications are common

>>INFECTIONS AND ABSCESSES- potential risk of spontaneous splenic rupture- infectious mononucleosis due to either Epstein-Barr virus or cytomegalovirus infection = small risk of spontaneous splenic

rupture- examples of possible causes of spon. Splenic rupture1. malaria2. listeria3. fungal4. dengue5. Q fever

6. Lymphoma7. Angiosarcoma8. Amyloidosis9. Pregnancy

- presumed pathophysiologic mechanism: infiltration of the splenic parenchyma w/ inflammatory cells, w/c distorts the architecture and fibrous support system of the spleen and thins the splenic capsule (in this setting: minor external trauma/Valsalva maneuver spontaneous splenic rupture)

- abscesses of the spleen: uncommon (0.14-0.7% based on autopsy findings); occur more frequently in tropical locations, where they are ssociated w/ thrombosed splenic vessels and infarction in px w/ sicle cell anemia

- 5 distinct mechanisms of splenic abscess formation:1. hematogenous infection2. contiguous infection3. hemoglobinopathy4. immunosuppression (inc. HIV, chemotherapy)5. trauma- presentation frequently delayed; Patients endure Sx for 16-22days before diagnosis- clinical manifestations1. fever2. LUQ pain3. Leukocytosis4. Splenomegaly- Dx confirmed by UTZ or CTscan (95% sensitivity and specificity)- Tx: broad spectrum antibiotics to more specific therapy (14days)- Splenectomy is the operation of choice (if cant be tolerated: percutaneous (successful for Px w/ unilocular disease) and open

drainage are options)

>>CYSTS AND TUMORS- Most common primary tumor of the spleen: Sarcoma- Cancer that most commonly spreads to the spleen: Lung Cancer- 0.6% rate of tumor metastasis to the spleen, mostly carcinomas (autopsy studies)

- parasitic vs. non parasiticParasitic Non Parasitic

- most common cause of splenic cysts worldwide- majority due to Echinococcus- more commonly found in areas where the pathogen is

endemic- Sx when present ar usually related to a mass lesion in

the LUQ or a lesion that impinges on the stomach

- most common: trauma (“pseudocyst”-because it doesn’t have a cellular lining

- less common examples:1. dermoid2. epidermoid3. epithelial cyst- may be symptomatic or asymptomatic

Dx:- ultrasound – can establish presence of cystic lesion; incidental finding of asymptomatic mass lesions- serologic testing – for echinococcal antibodies; can confirm or exclude the cystic lesion as parasitic (impt in planning operative

therapy)

Tx:- symptomatic parasitic cysts – splenectomy

Tx:- small symptomatic non parasitic cyst – excised with

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- avoidance of spillage of parasitic cyts contents into the peritoneal cavity to avoid anaphylactic shock

splenic preservation- asymptmatic – close observation w/ follow up ultrasound

to exclude significant expansion- large cyst – risk of cyst rupture with even minor trauma if

nonoperative management is used – may be unroofed- both operations may be done laparoscopically

>>Storage Diseases and Infiltrative DisordersGaucher's Diseas Niemann-Pick Disease Amyloidosis Sarcoidosis

Inherited lipid storage disorder characterized by the deposition of glucocerebroside in cells of the macrophage-monocyte system

Inherited disorder of abnormal lysosomal storage of sphingomyelin and cholesterol in the cells of the macrophage-monocyte system

Disorder of abnormal extracellular protein deposition

Inflammatory disease of young adults characterized by noncaseating granulomas in affected tissues

Underlying abnormality: deficiency in the activity of a lysosomal hydrolase;

Abnormal glycolipid storageorganomegaly (hepatomegaly, splenomegaly)

4 types (A,B,C, D): each w unique clinical presentations

lysosomal hydrolasetypes A and B = splenomegaly

Forms:Primary- associated w plasma cell dyscaria-splenic involvement (5% of cases)

Secondary-associated w chronic inflammatory conditions-may also present w large spleen

Any organ system may be involved;

Other affected tissues: lymph nodes, eyes, joints, spleen and heart

Sx:- early satiety- abdominal

discomfort**due to splenomegaly

- thrombocytopenia- normocytic anemia- mild leucopenia

**due to hypersplenism excessive sequestration of formed blood elements in the spleen

Other Sx:- bone pain- pathologic fractures- jaundice

Sx:- splenomegaly Sx

Sx:- splenomegaly Sx- maye range from

asymptomatic to multiorgan failure

Sx:- nonspecific- fatugue- malaise- splenomegaly (25%

of px)- massive

splenomegaly is rare (>1kg)

- Splenomegaly and/or hypersplenism Sx

Splenectomy alleviates hematologic abnormalities in px w hypersplenism but does NOT correct underlying disease process

Partial splenectomy – effective in children to correct both hematologic problems and Sx due to splenomegaly w/o incurring risk of overwhelming postsplenectomy sepsis

Splenectomy relieves splenomegaly Sx

Splenectomy effectively relieves Sx and corrects hematologic abnormalities such as anemia and thrombocytopenia

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>>MISC. DISORDERS AND LESIONSSplenic Artery Aneurysm Portal Hypertension Felty’s Syndrome

- rare- most common visceral artery

aneurysm- women 4x more likely to be

affected- usually arises in the middle to

distal portion of the splenic artery

- mortality is higher w/ px w potal hypertension (>50%) than those w/o it (17%)

- can result from numerous causes but usually due to cirrhosis

- splenomegaly and splenic cingestion often present sequestration and destruction of circulating cells in the spleen

- triad: rheumatoid arthritis, splenomegaly, neutropenia

- 3% of all px w/ rheumatoid arthritis (2/3 are women)

- immature complexes coat the surface of the WBCs sequestration clearance in the spleen neutropenia (<2000 neutrophils/mm3)

- neutropenia = risk for recurrent infections and often drives need to splenectomy

- spleen varies in size: from non palpable in 5-10% of px to massively enlarged in others

- spleen is 4x heavier than normal

Indications fot Tx:- presence of Sx- pregnancy- intentio to become pregnant- presence of pseudoaneurysms

associated w the inflammatory processes

Splenectomy not indicated for hypersplenism per se in Px w portal hypertension

- symptomatic neutropenia- transfusion dependent anemia- profound thrombocytopenia-

- aneurysm resection/ligation alone – for midsplenic artery lesions

- concomitant splenectomy – distal lesions in close proximity to the splenic hilum

- splenic artery embolization – but painful splenic infarction and abscess may follow; otherwise, excellent prognosis

- if splenectomy is required to bleeding from esophageal varices exacerbated by thrombocytopenia concomitant splenorectal shunt procedure (to decompress portal system)

- if secondary to splenic vein thrombosis – may be curable w splenectomy

- splenectomy if (+) bleeding from isolated gastric varices, normal liver function, hx of pancreatic disease (examine splenic vein thrombosis and treat w splenectomy if positive)

- corticosteroid, hematopoietic growth factors, methotrxate

- splenectomy- excellent prognosis

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V. Preoperative Considerations

Vaccination Splenic Artery Embolization Deep Vein Thrombosis Prophylaxis- imparts a small (<1-5%) but

definite lifetime risk of fulmitant, potentially life threatening infection

- vaccinations vs. encapsulated bacteria should be given at least 2 wks before surgery to protect against infections

- most common bacteria to cause serious infections in asplenic hosts: Streptococcus pneumoniae, H. influenzae type B, meninggococcus

- if spleen is removed emergentyly – like in trauma – vaccinations should be given asap after surgery w/ at least 1-2 days allowed for recovery

- after splenectomy – annual influenza immunization

Advantages- operative blood loss from

devascularized spleen- spleen size = easier

dissection and removal

Disadvantages- splenectomy related blood

loss- need for more analgesics- sometimes an extended

hospital stay- possibility of pancreatitis- risk of invasive arteriography

**author’s practice: pre-op embolization of spleens ≥20sm – allowed spleens >30cm to be resected laparoscopically w/ excellent conversion rate

- not infrequent after splenectomy esp if (+) splenomegaly and myeloproliferative disorders

- post splenectomy PVT:1. anorexia2. abdominal pain3. leukocytosis4. thrombocytosis

effective Tx:index of suspicion=early Dx w/ contrast enhanced Ct scan=start anticoagulation immediately

DVT prophylaxis:- sequencial compression

devices- SC administration of heparin

(5000 U)

VI. Splenectomy Techniques** Patient Preparation- vaccination- assess need for transfusions- optimization of preoperative coagulation status- blood typing- antibody screening tests- anemic px: transfused before surgery to a hemoglobin level of 10g/dL- thrombocytopenic px: should not undergo transfusion before the day or surgery and not before the intraoperative ligation of splenic artery- corticosteroid therapy px: give parenteral corticosteroid therapy perioperatively- DVT prophylaxis- after endotracheal intubation, na nasogastric (NG) tube is inserted for stomach decompression

>> LAPAROSCOPIC SPLENECTOMY Done in ELECTIVE Cases Standard approach for normosplenic px requiring splenectomy To come up with SMALLER Scars Put patient in the Right Lateral Decubitus (a midway “double” access” technique has also been advocated: px in

45-degree R lat. Decub) – and insert the Camera through the Umbilicus; requires 3-4 trochars; additional advantage over double access: exposure of vital anatomy in a manner that allows for a more intuitive sequence of dissection, paralleling that of OS)

Double access technique:requires the placement of 5-6 trochars Angled 30 or 45-degree laparoscope (2mm, 5mm,10m)

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Placement f trochars in the LUQ should be performed under laparoscopic visualization

>> OPEN SPLENECTOMY Done in EMERGENCY Cases – Most Commonly Indicated for Traumatic Rupture of the Spleen Other scenarios: massive splenomegaly, ascites, portal hypertension, multiple prior operations, extensive

splenic irradiation, possible splenic abscess Risk of INFECTIONS! Px: supine position w the surgeon ath the patient’s right Left subcostal incision paralleling the left costal margin and lying 2 fingerbreadths below it – preffered for most

elective splenectomies Midline incision – optimal for exposure when spleen is ruptured/massively enlarged/abdominal abcess is needed

for a staging laparotomy for Hodgkin’s disease Thoracoabdominal incision – rarely used – may be necessary for access to a challenging/significantly enlarged

spleen Incision of lateral peritoneal attachments (most notably the splenophrenic ligament)– further medial mobilization of

the spleenindividual ligation and sequential division of short gastric vesselssplenic hilar dissection (artery first then vein; be careful not to injure the pancreas)division

Once the spleen is excised, hemostasis is secured by irrigating and suctioning and inspecting the bed of dissection (splenic bed not routinely drained)completion of surgeryremove nasogastric tube

Spleen is mobilized by dividing ligamentous attachments, usually beginning with the splenocolic ligament (+)significant splenomegaly achieve lesses sac access through gastrosplenic or gastrohepatic attachments

ligate plenic artery in continuity along the superior border of the pancreas- allows safer manipulation of the spleen- safer dissection of the splenic hilum- facilitates some shrinkage af the spleen- provides an autotransfusion of erythrocytes and platelets

>> PARTIAL SPLENECTOMY- indicated o minimize the risk of postsplenectomy sepsis in children- others: certain lipid storage disorders (Gaucher’s) and some forms of traumatic splenic injury (blunt and

penetrating)- laparoscopic or open- spleen must be mobilized and the splenic hilar vessels attached to the targeted segment ligated and divided;

devascularized segment of the spleen=transected along an obvious line of demarcation- limited bleeding from the cut surface= controlled by cauterization, argon coagulation, or application of direct

hemostatic agents (cellulose gauze, fibrin glue)

>> INADVERTENT INTRAOPERATIVE SPLENIC INJURY- true incidence is unknown- risk of death, significant short term morbidity, blood loss, need for transfusion,hospital stay- linked to gastric fundoplication, colectomy, paraesophageal hernia repair, nephrectomy, abdominal and pelvic

vascular surgery, some reports of colonoscopy- most common mechnism: improper traction on the spleen against its peritoneal attachments- most common type of injury: capsular tears- parenchymal lacerations and subcapsular hematomas may also occur- lower pole more commonly injured

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VII. Splenectomy Outcomes>> COMPLICATIONS OF SPLENECTOMY

A. Pulmonary Complicationso Atelectasis of Left Lung Lobe = MOST Common Complication (16% of Patients after Open

Splenectomy)o Pleural Effusion and Pneumonia

B. Hemorrhagic Complicationso Bleeding – usually occurs Intraoperativelyo Occasionally presents as a SUBPHRENIC HEMATOMA Post-Op o Be careful with the Small Gastric Vessels to avoid Brisk Bleeding

C. Infectious Complicationso Infections = OPSS, Wound Infections, Subphrenic Abscesso OPSI / OPSS (Overwhelming Post-Splenectomy Infection) = Streptococcus pneumonia o Other Causes include = H. influenza, Meningococcemia, E.coli

D. Pancreatic Complicationso Because the Tail is abuting to the Spleen, if we may accidentally Cut the Tail of the Pancreas, leading

to Fistula Formation (Intraoperative Trauma to the Pancreas – especially the Tail)o Others: Pancreatitis, Pseudocyst, Pancreatic Fistula

E. Thromboembolic Complicationso Deep Vein Thrombosis (DVT) = occurs in 5-10% of Patients undergoing Splenectomyo For DVT Prophylaxis = HEPARIN is recommended routinely

>> HEMATOLOGIC OUTCOMES- discussed =)

VIII. OVERWHELMING POSTSPLENECTOMY INFECTION (OPSI / OPSS) The Loss of the Spleen’s Ability to Filter and Phagocytose Bacteria and Parasitized Blood Cells

prediposes the Patient to Infection by Encapsulated Bacteria of Parasites Reason for splenectomy – single most influencial determinant of OPSI risk 3 factors: 1) loss of splenic macropahges 2)diminished tuftsin production 3)loss of the spleen’s

reticuloendothelial screening function It is the MOST POTENTIALLY FULMINANT Complication in Splenectomy Most Common Cause = Streptococcus pneumoniae (50-90% of Cases) Examples: S. pneumoniae, H. influenzae, Neisseria meningitides (classic examples); others- grp A strep,

enterococcus, bacteroides, salmonella, bartonella Infections w protozoa that invade RBCs: Babesia microti (tick bites), Ehlichia Plasmodium – infections

occur more frequently in splenectomized px than normal hosts

A. Clinical Manifestations of OPSI / OPSS o Fevero Fatigueo Head and Body Acheo Diarrheao Abdominal Paino Hypotensiono Septic Shocko Disseminated Intravascular Coagulation

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B. Treatmento POLYVALENT VACCINEo Antibiotic therapy – considered in 3 contexts: deliberate therapy for established/presumed infections,

prophyaxis in anticipation of invasive procedures, general prophylaxis; daily doses of antibiotics until 5yrs ar atleast 5 yrs after splenectomy**IMPORTANT Notes: (jaime’s)

Elective Case (Scheduled Splenectomy) = give Vaccines TWO WEEKS Before the Schedule Emergency Splenectomy = give Vaccines WITHIN 2 DAYS Post-Op (after the Splenectomy)

-------- NOT in the textbook =) or at least not discussed in the same order heheV. SPLENECTOMY AS A TREATMENT OF CHOICE (This will come out in the Test)

Hereditary Spherocytosis Splenic Cysts and Tumors Splenic Abscess Splenic Artery Aneurysm Massive Splenic Injury (Grade-IV)

SOME CONDITIONS OF THE SPLEEN Splenic Abscess Splenic Cysts Abdominal Trauma

I. SPLENIC ABSCESS Most Cultures will Reveal = Staphylococcus and Streptococcus Potential risk of Spontaneous Splenic Rupture (Epstein-Barr Virus or Cytomegalovirus Infectious

Mononucleosis increased risk of spontaneious splenic rupture) It is a RARE Condition that is commonly Missed (a high index of suspicion is needed) Routes of Abscess Formation:

Hematogenous (Most Common) Osteomyelitis, Pyelonephritis, Endocarditis, IV-Drug AbuseContiguous Pancreatic Fistulas, Colonic Malignancies invading Colonic WallImmunosuppression HIV/AIDS Patients; those undergoing ChemotherapyTrauma Penetrating Splenic Trauma

A. Clinical Presentation of Splenic Abscesso High Grade Remittent Fevero Leukocytosis (increase WBC)o Splenomegalyo Left Upper Quadrant Abdominal Paino Left Shoulder Pain

**NOTE: A Spleen which is 2-3x of its Normal Size = SPLENOMEGALY (it is PALPABLE)! Splenomegaly is usually seen in the first 2-Weeks of the Condition

B. Diagnostics:1. CT-Scan

Standard Diagnosis! (+) Unilocular Abscess Cavity Shows Low Density Lesion (in Contrast CT-Scan)

2. X-Ray (+) Left Diaphragmatic Elevation (sometimes as high as 5cm) (+) Left Pleural Effusion

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C. Treatmento Broad Spectrum Antibiotics = Cephalosporins (based on the Cultures)o CT-Scan or Ultrasound Guided Percutaneous Drainageo Open Drainageo SPLENECTOMY = Gold Standard

**NOTE: Staphylococcus and Streptococcus = PREDOMINANT Microbes identified

II. SPLENIC CYSTSA. Two Main Classification = TRUE + PSEUDOCYST

1. Primary Cysts (True) Non-Parasitic (Congenital + Neoplastic) Parasitic

2. Secondary Cyst PSEUDOCYST

B. Cysts and Tumors of the SpleenEchinococcal Cysts Most Common TRUE PARASITIC Splenic Cyst!

Hemangioma Most Common BENIGN Tumor

Non-Hodgkin’s Lymphoma Most Common PRIMARY MALIGNANT Tumor

Splenic Hematoma Most Common PSEUDOCYST (Secondary Cyst)

Epidermoid Cyst Most Common TRUE NON-PARASITIC Splenic Cyst

**NOTE: Lung Cancer = Most Common Malignancy that Metastasizes to the Spleen!

III. ABDOMINAL TRAUMA In BLUNT Abdominal Trauma, the MOST COMMONLY Injured Organ is the SPLEEN Trauma to the Spleen = Seen in Vehicular Accidents, Gunshot Wounds, Stab Wounds

A. Splenic Injury Scale (1994)GRADE DESCRIPTION MANAGEMENT (prenotes)

I Hematoma < 10% Surface AreaLaceration < 1cm Deep

Non-Operative

II Hematoma 10-15% Surface AreaLaceration 1-3cm Deep

Non-Operative

III Hematoma > 50% or ExpandingLaceration > 3cm Deep

Operative

IV Laceration Segmental or Hillar Vessels Operative

V Laceration SHATTERED Spleen Operative

**NOTE: The Gravity of the Injury INCREASES as the Grade Increases Grade I = GOOD Prognosis Grade V = WORST Prognosis!

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B. Clinical Manifestations of Patients with Splenic Injurieso PALLOR (Pale Looking Patient)o Vital Signs Deterioration (Tachycardia, Hypotension)o Abdominal Findings (Silent Abdomen, Abdominal Fullness, Tenderness & Quarding)

**NOTE: To Assess Pallor Compare your Palm with the Patient Also look at the Palpebral Conjunctiva

C. Diagnostic Testso Serial CT-Scano Ultrasonographyo Serial Hemoglobin and Hematocrit Determinationo Diagnostic Peritoneal Lavage (DPL)

**NOTE: Mainstay is Serial CT-Scan + Serial Ultrasound

D. Management of Splenic Injurieso Grade I and II = NON-OPERATIVE Managemento Grade III, IV, and V = ICU Observation; SURGERY!

**Criteria for NON-OPERATIVE Management: Stable Vital Signs CT-Scan Documenting Exact Injury Absence of Progressive Bleeding Peritonitis Absence of Concomitant Intraabdominal Injuries Blood Transfusion (< 2 Units / 24 Hours)

E. Techniques for Splenic Salvage1. Individual Bleeding Vessel Ligation

If the Hematoma is SHALLOW We can Cauterize the Vessel

2. Cautery or Hemostatic Agent Application Burning (with the use of Electricity) the Parenchyma of the Spleen Hemostatic Agents = absorbs blood and leads to Coagulation

3. Splenorrhapy Repairing / Mesh = Wrap the Spleen (especially if Grade-II or III) To affect Hemostasis, we do Tightening of the Mesh to Save the Spleen

4. Partial Splenectomy Removal of just the Upper or Lower Pole of the Spleen

5. Splenic Autotransplantation Cut a piece of Spleen, and Imbed it in the Omentum A fragment of spleen is cut and transplanted into the Greater Omentum Vascularization will occur, resulting in a FUNCTIONAL Spleen

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